Thyroid vascularity and blood flow are not dependent on serum thyroid hormone levels: studies in vivo by color flow doppler sonography.

OBJECTIVE Thyroid blood flow is greatly enhanced in untreated Graves' disease, but it is not known whether it is due to thyroid hormone excess or to thyroid hyperstimulation by TSH-receptor antibody. To address this issue in vivo patients with different thyroid disorders were submitted to color flow doppler sonography (CFDS). SUBJECTS AND METHODS We investigated 24 normal subjects, and 78 patients with untreated hyperthyroidism (49 with Graves' hyperthyroidism, 24 with toxic adenoma, and 5 patients with TSH-secreting pituitary adenoma (TSHoma)), 19 patients with thyrotoxicosis (7 with thyrotoxicosis factitia, and 12 with subacute thyroiditis), 37 euthyroid patients with goitrous Hashimoto's thyroiditis, and 21 untreated hypothyroid patients with Hashimoto's thyroiditis. RESULTS Normal subjects had CFDS pattern 0 (absent or minimal intraparenchimal spots) and mean intraparenchimal peak systolic velocity (PSV) of 4.8+/-1.2cm/s. Patients with spontaneous hyperthyroidism due to Graves' disease, TSHoma, and toxic adenoma had significantly increased PSV (P<0.0001, P=0.0004, P<0.0001 respectively vs controls) and CFDS pattern. Patients with Graves' disease had CFDS pattern II (mild increase of color flow doppler signal) in 10 (20%) and pattern III (marked increase) in 39 cases (80%). Mean PSV was 15+/-3cm/s. Patients with toxic adenoma had CFDS pattern I (presence of parenchymal blood flow with patchy uneven distribution) in 2 (8%), pattern II in 16 (70%) and pattern III in 5 (22%). Mean PSV was 11+/-2.4cm/s. Patients with TSHoma showed CFDS pattern I in one case (20%) and pattern II in 4 (80%). Mean PSV was 14.8+/-4.2cm/s. Patients with thyrotoxicosis had normal PSV (4.2+/-1. 1cm/s in subacute thyroiditis, 4+/-0.8cm/s in thyrotoxicosis factitia, P=not significant vs controls) and CFDS pattern 0. Untreated euthyroid patients with goitrous Hashimoto's thyroiditis had CFDS pattern 0, and mean PSV (4.3+/-0.9cm/s; P=not significant vs controls). Untreated hypothyroid patients with goitrous Hashimoto's thyroiditis had CFDS pattern I in 14 cases (67%), pattern II in 4 (19%) and pattern 0 in 3 (14%) and mean PSV (5.6+/-1. 4cm/s) was higher than that of controls (P=0.026). CONCLUSIONS An increase in both intrathyroidal vascularity and blood velocity was observed in patients with spontaneous hyperthyroidism but not in thyrotoxicosis due to either ingestion of thyroid hormones or to a thyroidal destructive process. The slightly increased vascularity and blood velocity observed in patients with hypothyroid Hashimoto's thyroiditis suggests that thyroid stimulation by either TSH-receptor antibody or TSH is responsible for the increased thyroid blood flow.

[1]  W. Degroot,et al.  Hyperthyroidism as a high cardiac output state. , 1970, American heart journal.

[2]  T. Rago,et al.  Color flow doppler sonography in thyrotoxicosis factitia , 1996, Journal of endocrinological investigation.

[3]  A. Pinchera,et al.  Low serum thyroglobulin as a clue to the diagnosis of thyrotoxicosis factitia. , 1982, The New England journal of medicine.

[4]  J. Patterson,et al.  MECHANISM OF CERTAIN ABNORMALITIES OF THE CIRCULATION TO THE LIMBS IN THYROTOXICOSIS. , 1965, The Journal of clinical investigation.

[5]  K. Wolf,et al.  Appearance of thyroid diseases using colour-coded duplex sonography. , 1989, European journal of radiology.

[6]  K. Burman,et al.  Endothelin binding to receptors and endothelin production by human thyroid follicular cells: effects of transforming growth factor-beta and thyrotropin. , 1993, The Journal of clinical endocrinology and metabolism.

[7]  H. Shimokawa,et al.  Endothelium‐Derived Relaxing Factor and Coronary Vasospasm , 1989, Circulation.

[8]  T. Ishigaki,et al.  Thyroid nodules: evaluation with color Doppler ultrasonography , 1993, Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine.

[9]  P. Ladenson Recognition and management of cardiovascular disease related to thyroid dysfunction. , 1990, The American journal of medicine.

[10]  F. Bayard,et al.  Regulations of vasculatropin/vascular endothelial growth factor bioavailability. , 1994, Hormone research.

[11]  C. Bartolozzi,et al.  Color flow Doppler sonography rapidly differentiates type I and type II amiodarone-induced thyrotoxicosis. , 1997, Thyroid : official journal of the American Thyroid Association.

[12]  M. Surks,et al.  Effects of thyroid hormone on left ventricular function in patients treated for thyrotoxicosis. , 1981, The American journal of cardiology.

[13]  K. P. Lee,et al.  Color-flow Doppler sonography in Graves disease: "thyroid inferno". , 1988, AJR. American journal of roentgenology.

[14]  E. S. Brannon,et al.  A correlative study of the cardiac output and the hepatic circulation in hyperthyroidism. , 1950, The Journal of clinical investigation.

[15]  Elena S. Di Martino,et al.  Thyroid blood flow evaluation by color-flow doppler sonography distinguishes Graves’ disease from Hashimoto’s thyroiditis , 1995, Journal of endocrinological investigation.

[16]  M. Baldini,et al.  Color Doppler sonography in Graves' disease: value in assessing activity of disease and predicting outcome. , 1996, AJR. American journal of roentgenology.

[17]  I. Klein,et al.  Thyrotoxicosis and the heart. , 1998, Endocrinology and metabolism clinics of North America.

[18]  P. Nicod,et al.  The Thyroid and the Heart , 1993, Circulation.

[19]  F. Cetani,et al.  TSH receptor and disease , 1996, Clinical endocrinology.